Assessment of antioxidant activity of eugenol in vitro and in vivo.
Assessment of antioxidant activity of eugenol in vitro and in vivo.
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DOI:
10.1007/978-1-60327-029-8_10
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发表时间:
2010
期刊:
影响因子:
--
通讯作者:
Nakka, Lakshmaiah
中科院分区:
文献类型:
--
作者:
Nagababu, Enika;Rifkind, Joseph M.;Boindala, Sesikeran;Nakka, Lakshmaiah
Reactive oxygen species are implicated in many human diseases and aging process. Much of the evidence is based on experimental data indicating increasing rates of lipid peroxidation in disease states and the ameliorating effects of antioxidants. It is becoming increasingly evident that the natural antioxidants, which have basically a phenolic structure, play an important role in protecting tissues against free radical damage. Eugenol (4-allyl-2 methoxyphenol), is one among such naturally occurring phenolic compounds. The antioxidant activity of eugenol is evaluated by the extent of protection offered against free radical mediated lipid peroxidation using both in vitro and in vivo studies. The in vitro lipid peroxidation is induced in mitochondria by (Fe(II)-ascorbate) or (Fe(II) + H2O2). The lipid peroxidation is assessed colorimetrically by measuring the formation of thiobarbituric acid reactive substances (TBARS) following the reaction of oxidized lipids with TBA. Eugenol inhibits both iron and Fenton reagent mediated lipid peroxidation. The inhibitory activity of eugenol is about five fold higher than α-tocopherol and about ten fold less than the synthetic antioxidant, BHT. The in vivo antioxidant activity of eugenol is evaluated by the determination of certain biochemical parameters (SGOT, Cyt.P450, glucose-6-phosphatase), peroxidation products and histopathological examination of •CCl3 radical induced hepatotoxicity in rats. Eugenol significantly inhibits the rise in SGOT activity and cell necrosis without protecting the endoplasmic reticulum (ER) damage as assessed by its failure to prevent a decrease in glucose-6-phosphatase activity. The protective action of eugenol has been found to be due to interception of secondary radicals derived from ER lipids rather than interfering with primary radicals of CCl4 (•CCl3/CCl3OO•).
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影响因子:
3.3
作者:
NAGABABU, E;SESIKERAN, B;LAKSHMAIAH, N
通讯作者:
LAKSHMAIAH, N
DOI:
10.1080/j157v04n04_03
发表时间:
2004-01-01
期刊:
Journal of Herbal Pharmacotherapy
影响因子:
--
作者:
Singh, U. P.;Singh, D P.;Singh, R. B.
通讯作者:
Singh, R. B.
影响因子:
4.2
作者:
Scalbert, A;Williamson, G
通讯作者:
Williamson, G
影响因子:
15.9
作者:
KARMEN, A;WROBLEWSKI, F;LADUE, JS
通讯作者:
LADUE, JS
影响因子:
3.3
作者:
NAGABABU, E;LAKSHMAIAH, N
通讯作者:
LAKSHMAIAH, N